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Allergol Immunopathol (Madr). 2008 Jul-Aug;36(4):215-27.

Immunopathological mechanisms of eosinophilic oesophagitis.

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  • 1Department of Gastroenterology. Complejo Hospitalario La Mancha Centro. Alcázar de San Juan-Tomelloso. Ciudad Real. Spain.



Eosinophilic oesophagitis (EO) is a chronic inflammatory disease of the oesophagus, with an emergent character, defined by the presence of a dense infiltrate by eosinophilic leukocytes restricted to the mucosa of this organ after excluding gastro-oesophageal acid reflux. It is manifested by chronic and/or recurrent dysphagia and episodes of oesophageal alimentary impaction, with great variation in terms of intensity, frequency, and duration of the attacks.


An Internet-based search was performed for the most recent articles with relevant information concerning immunopathological mechanisms involved in EO.


Bibliographical data allow us to define that EO is related to an allergic or hypersensitivity-induced reaction after exposure to foods or inhalants, with increased prevalence of sensitisation to these allergens. Data published up to now suggest a cellular hypersensitivity reaction rather than a humoral one in the physiopathology of EO. In this disease, sensitised T-lymphocytes mediate a Th2 type response, releasing cytokines such as IL-5, with a possible Th1 component that requires further investigation. The function of the abundant CD8+ T-lymphocytes present in the oesophageal epithelium has yet to be explained. Mast cells also participate in epithelial inflammatory infiltrate in EO, and it is still unknown if its activation, mainly through IgE, contributes to the immunopathology of the disease even though EO rarely manifests immediate hypersensitivity reactions. IL-5 and different forms of eotaxins perform an important active role in the recruitment of eosinophils to the oesophagus.


EO is an immunologically complex and little studied entity that is associated with other allergic diseases and in which different effector cells participate, determining an immunological response of cellular rather than a humoral hypersensitivity reaction. The data available point out that EO is a disorder of the Th2 retarded immune response, in which the triggering factor might not be IgE. Although the final inflammatory phenomena observed in EO are common for the different patients, the cascade of inflammatory mediators that lead to them might not be identical in all cases, and the morphological and functional disorders observed in EO would represent the final convergence of different activation forms of the mechanisms of inflammation.

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